Schizophrenia Due date

Schizophrenia Due date

Schizophrenia

Duedate

Schizophrenia

Overthe past several years, clinical research has increasingly revealedheterogeneity and marked morbidity of mental disorders. Recentresearch has demonstrated a significant correlation between psychoticdisorders and heterogeneity. Numerous psychological disorders havebeen largely said to emanate from genetic composition. According toDelisi (2008), a vivid example of such disorders is schizophrenia.The intent of this paper is to offer an explicit view ofschizophrenia as a psychological disorder.

Psychologistsclassify schizophrenia as a prevalent disorder across all age groups.As a clinical syndrome, schizophrenia is a disabling psychiatricdisorder that often leads to withdrawal, in ability to makedecisions, poor concentration and disturbances in terms ofperception. Moreover, male patients diagnosed with schizophrenia haveexhibited olfactory disturbances .The correlation between particulargenes and certain neuropsychiatry diseases is unclear. However,scientific research regarding this subject is evolving at a rapidspeed. Pleiotrophic effects, epitasis and partial penetrance are someof the neuroanatomical pathways attributed with the cause ofschizophrenia. Evidently, these pathways believed to causeschizophrenia have instigated much debate in the clinical field.

Therehave been different assertions associated with the causes ofschizophrenia. Some medical practitioners assert that schizophreniaresults from genetic composition while others postulate thatschizophrenia results from prenatal development and early childhooddevelopment. However contemporary research on schizophrenia is basedon neuroanatomical model. Here, physicians view schizophrenia as asyndrome rather than as a single disease due to its complicatedsymptoms.

Accordingto Harvey (2012), schizophrenia results from a combination of geneticvulnerability and environmental factors. However, there is alsoavailable research stating that all cases of schizophrenia do notresult from heredity. Some of the people who possess schizophrenicgenes may not suffer from schizophrenia. Recent research posits thatrisk for schizophrenia due to heredity is 80%. this implies that notall schizophrenic cases result from genetic vulnerability.

Studieson families indicate that the closer a person is to a schizophrenicpatient, the higher the chances of suffering from the disorder. Theage of the father plays a major role in the cause of schizophrenia.High paternal age increases the chances of mutations in the cellchromosomes where sperms are produced. This increases the copyingerror in the replication of the DNA. As a result, there is anincrease in cell divisions which in turn cause an increase in thenumber of mutations that are known to cause schizophrenia.

Otherstudies have also revealed that rare deletions and replications ofminute sequences of DNA in genes are major causes of schizophrenia.It should be noted that these copy number variations as well asneuraoanatomical pathways are not linked to families withschizophrenic cases. This implies that these deletions and DNAduplications result from homologous cell combinations. It has alsobeen speculated that copy number variations contribute to epigeneticswhich plays a central role in the cause of schizophrenia.

Astudy conducted in 2008 among 2977 patients suffering fromschizophrenia, revealed that copy number variations in gene deletionsresulted to cases of schizophrenia. This depicts that schizophreniamay not necessarily be linked to family history of schizophrenia.Individual deletion of homologous genes may as well lead toschizophrenia. Moreover, current research has postulated thatschizophrenia may emanate from other psychiatric disorders. Thisdepicts that a patient suffering from a different psychiatricdisorders stands a potential risk to suffer from schizophrenia.According to Diben et al (2009), genetic overlap between genes thatcause bipolar, autism spectrum disorder and attention deficithyperactivity disorder may instigate schizophrenia among suchpatients.

Itis worth noting that schizophrenia has a prevalence of nearly 1%.Various pharmacological treatments have been developed in a bid totreat and reduce the effect of schizophrenia. The invention ofclozapine and chlorpromazine marked a major milestone inschizophrenia pharmacotherapy. Over the years, various antipsychoticshave been developed. Their development has greatly enhanced thecomprehension of neuropharmacology of schizophrenia.

Despitethe available pharmacological treatments, many schizophrenic symptomshave not responded to these treatments. In the recent past, numerouspharmacological approaches have been advanced to improve thesemedications. Such treatments methods include, serotonin receptor,dopamine receptor and neuron protection modulations. Thesemodulations are based on the hypothesis that schizophrenia entailsneurotransmission and dopaminergic forces in the brain circuits.These activities hinder the brain receptors from performing theirphysiological functions. The treatment methods are therefore beingdesigned to improve the D2 receptors in both G-Protein dependent andindependent signaling (DeLisi, 2008).

Inconclusion, schizophrenia is widely depicted as a psychiatricdisorder rather than a mental sickness. This is because its symptomsare not clearly revealed and also the the causes of the syndrome arenot clearly comprehended. Physicians argue that the causes of mentalsicknesses are well understood. The potential behavior of mentallyill patients is also predictable. However, schizophrenia remainsunclear to majority of the medical practitioners in the world. As aresult, schizophrenia cannot be classified as a mental illness butrather as a syndrome.

References

DeLisi, L.E . (2008). The concept of progressive brain change inschizophrenia: Implications for understanding schizophrenia.SchizophreniaBulletin , 34 , 312– 321

Dibben, C.R. , Rice , C. , Laws , K. &amp McKenna , P.J . (2009) . Isexecutive impairment associated with schizophrenic syndromes? Ameta-analysis. PsychologicalMedicine , 39 ,381 392 .

Frith, C.D . (1992) . TheCognitive Neuropsychology of Schizophrenia .Hove:Erlbaum

Harvey, P.D . (2012) . Cognitive impairment in schizophrenia:

Profile, course, and neurobiological determinants. Handbookof Clinical Neurology , 106 , 433– 445.

JavittD.(1991). Recent advances in the phencyclidine model ofschizophrenia.AmJ Psychiatry 148: 1301–1308.